Traumatic Hyphema

Pathogenesis and Management

FRED M. WILSON II, MD

0> Abstract: Traumatic hyphema is a potentially serious problem, but the

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UJ overall prognosis is good unless associated injuries are severe. Medical
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:2 treatment is of little value for hyphema itself but is useful for complications.
::> Surgical treatment is hazardous and should be resorted to only in select
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• circumstances. Severity of injury is more important than is treatment in
determining the outcome . Practitioners should not feel obliged to use
ritualistic therapy that they consider to be of uncertain value. [Key words:
angle recession, corneal blood staining, hemorrhage, hyphema, trauma,
traumatic cyclodialysis, traumatic glaucoma.] Ophthalmology 87:910-919,
• 1980
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CD Hyphema is the presence of blood in the an- of intraocular pressure in an inflammed eye.!
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UJ terior chamber. Tiny hemorrhages may be visi- This paper deals with traumatic hyphema and
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UJ ble only with the slit lamp, in the form of eryth- my approach to its management based on per-
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rocytes floating and circulating in the aqueous sonal experience, available evidence, and what
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>- humor. Slightly larger amounts of blood settle I consider to be currently valid opinion.
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o the iris, lens, or vitreous. Still larger hemor-
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rhages gravitate to the inferior aspect of the CLASSIFICA TION
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anterior chamber, producing a grossly visible,
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I "layered" hyphema. The most severe hemor- Classification of hyphemas in terms of sev-
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o rhages can fill the anterior chamber; these tend eral variables is useful for evaluating severity of
to clot, probably because of impaired circula- injury, prognosis, and management. The most
tion of aqueous, and nearly always produce important variable is the amount of blood,
glaucoma. Total, clotted hyphemas are dark which is best classified according to the scheme
brown, purple, or black and are referred to of Edwards and Layden. 2 My classification
as "black-ball" or "eight-ball" hemorrhages (Table 1) is otherwise a modification and expan-
(Fig 1). sion of one proposed by Lebekhov and Iandiev. 3
Causes of hyphema include trauma, surgery,
neoplasms, vascular anomalies, neovasculari-
zation, blood dyscrasias, and sudden lowering
PATHOPHYSIOLOGY

From the Corneal and External Ocular Disease Ser-
vice , Department of Ophthalmology, Indiana Univer-
sity School of Medicine, Indianapolis.
Presented at the Eighty-Fourth Annual Meeting ,
American Academy of Ophthalmology, San Fran-
cisco, November 5 - 9, 1979.
Supported in part by a grant from Research to Prevent
Blindness, Inc., New York.
Reprint requests to Dr. Wilson, Department of
Ophthalmology, Indiana University School of
Medicine, 1100 West Michigan Street, Indianapolis, IN
47223.
SOURCE OF HEMORRHAGE
Intraocular bleeding can be caused by lacera-
tions or ruptures of the ocular coats, but most
traumatic hyphemas occur after blunt, contu-
sive injuries to the eye. Indentation of the an-
terior surface of the eye causes a sudden rise in
pressure in the anterior chamber, stretching of
the limbal tissues, posterior and peripheral
movement of aqueous, and retrodisplacement
of the iris and lens. The result can be a tear in
the ciliary body or iris, usually in the area of the
angle4 (Fig 2).

910 0161-6420/S0/0900/0910/$01.00 © American Academy of Ophthalmology

Fig 1. "Black-ball" hy-
phema. Dark, clotted blood
fills the anterior chamber
and obscures the iris.

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Table 1. Classification of Nonsurgical ing, occurring in perhaps 71 to 94% of all w
I
Traumatic Hyphema * cases. 5- 7 The circular and oblique muscle fibers Il..
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Etiology of the ciliary body are torn from the longitudinal o
Contusion (meridional) fibers, which remain attached to I--
the scleral spur (Fig 3).8 The injury disrupts the «
Laceration or rupture ~
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Origin major arterial circle of the iris, arterial branches «a:
Iris sphincter or stroma to the ciliary body, recurrent choroidal arteries, I--
Iris root (iridodialysis)
Ciliary body face (angle recession)
or veins coursing between the ciliary body and
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•
episcleral venous plexus.9 Healing of this kind o
Ciliary body disinsertion (cyclodialysis) of injury results in postcontusion deformity of (j)
--l
Vascular anomalies or neovascularization
Vitreous hemorrhage (with spillover to anterior the angle, which is characterized by localized :s:
chamber) deepening of the anterior chamber and by
Type equatorial and posterior retraction of the angle
Primary recess, the iris root, the anterior ciliary pro-
Secondary (rebleed) cesses, and the circular and oblique fibers ofthe
Continual ciliary muscle. 8 •10 The ciliary body loses its
Volumet normal wedge shape and becomes fusiform. 8
Grade I (less than one-third of anterior chamber) Traumatic cyclodialysis (Figs 2, 4) is occa-
Grade II (one-third to one-half of anterior chamber) sionally responsible for hyphema. 9 The longitu-
Grade III (greater than one-half of anterior chamber) dinal fibers of the ciliary muscle are separated
Duration
Acute (1-7 days)
completely from the scleral spur, producing a
Subacute (7-14 days) cleft in the supraciliary space (Fig 4).8
Chronic (over 14 days) Iridodialysis (disinsertion of the root of the
Character iris) and tears of the iris stroma or sphincter are
Liquid (red) uncommon as causes of hyphema, as these in-
Clotted (brown or black) juries generally cause little or no bleeding. 9
Mixed Abnormal blood vessels of the iris or cornea
Organized (tan, gray, or white) are another possible source of traumatic
Patient hyphema. Blood in the vitreous can find its way
Normal into the anterior chamber if the eye is aphakic
Clotting disorder
Sickling hemoglobinopathy or has a subluxated lens.

* Modified and expanded from Lebekhov and landiev. 3

t From Edwards and Layden!
A tear in the anterior face of the ciliary body
(also known as traumatic recession ofthe angle;
Figs 2, 3) is the most common source of bleed-
ABSORPTION OF HEMORRHAGE
Blood leaves the anterior chamber by way of
the trabecular meshwork, and the juxtacanalic-
ular tissue, or Schlemm's canal. Jl - 16 The iris is
probably insignificant as a source of absorption
of blood,12 although it can be a source of
fibrinolysin. 15 ,17 Fibrinolysin is important in

911
 Fig 2. Usual pathogenesis of traumatic hyphema. Ocular contusion indents cornea, raises intracameral pressure, and pro-
duces tear in anterior face of ciliary body (left arrow) or cyclodialysis (right arrow). Modified from a concept of R. N. Shaffer,
MD, San Francisco, as cited by H. D. Hoskins, MD.4

freeing erythrocytes from fibrin clots, so that and that of others,23,24 indicate that the overall
the red blood cells can escape by way of the incidence of rebleeding is probably about 20 to
meshwork. 25%. Most secondary hemorrhages occur from
two to five days after the initial injury, and
SECONDARY HEMORRHAGE
nearly all occur before the seventh day.7· 19 ,2o,24
Secondary hemorrhages (" rebleeds") occur The pathogenesis of rebleeding is not known.
• in 0 to 65% of patients with traumatic hyphema, It may be related to fibrinolysis and retraction
o
OJ depending on the extent of the initial hemor- of clots 15 .20 ,21 or to bleeding of fragile new
capillaries. 25 Rebleeds are sometimes multiple
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rhage, the treatment, and the series of patients
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Fig 3. Tear in anterior face of ciliary body (traumatic recession of the angle; arrow). Longitudinal ciliary muscle fibers (L)
remain attached to scleral spur. Note blood (B) in anterior chamber (hematoxylin and eosin x 30).

912
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Fig 4. Traumatic cyclodialysis. The ciliary body (C) is separated completely from the scleral spur, producing a cleft in the
supraciliary space (S) (hematoxylin and eosin x 30). •
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the full thickness of the stroma and can cause ~

COMPLICATIONS
Aside from associated mJuries, the major
complications of traumatic hyphema are
glaucoma and blood staining of the cornea
(Table 2).
A recently emphasized cause of glaucoma
with hyphema is obstruction of aqueous outflow
by sickled erythrocytes. Goldberg29 has shown
that patients with hyphema and sickling hemo-
globinopathies (AS, SC, and perhaps others)
can have a higher percentage of sickled eryth-
rocytes in the anterior chamber than in the
peripheral blood and that such patients are apt
to develop glaucoma with relatively small
hyphemas. These patients seem also to be
highly susceptible to optic-nerve damage, and
even to occlusion of the central retinal artery,
after only mild or moderate elevations of in-
traocular pressures.
Blood staining of the cornea is the result of
impregnation of the corneal stroma by .hemo-
globin and small amounts of hemosiderin (Fig
5).8 The stroma shows rust-brown discoloration
and loss of normal relucency (Fig 6), seen first
only in the deep stroma and only with the aid of
the slit lamp. Later, blood staining can affect
substantial loss of vision (Fig 7). Factors that
predispose to the development of blood staining
are: (1) a large amount of blood in the anterior
chamber;23.3o (2) prolonged duration of
hyphema;30,31 (3) increased intraocular pres-
sure,23,30 and (4) dysfunction of the corneal en-
dothelium. 23 ,3o
PROGNOSIS
The larger the hyphema, the worse the prog-
nosis. Small hyphemas usually disappear within
four or five days.24 Those that occupy half or
more of the anterior chamber (grade II or III)
are more likely to be associated with delayed
clearing, glaucoma, blood staining, rebleeding,
and poor visual resuits. 2,22
The chance of recovering visual acuity of
20150 or better is 75-90% with grade I
hyphemas ;2,24 65 - 70% with grade II ;2,24 and
25-50% with grade III.2,23,24 About 25% of pa-
tients with grade I hyphemas experience sec-
ondary hemorrhages, as compared with 65% of
those with grade III.2
Rebleeding worsens the prognosis,4,19,32 but
only because secondary hemorrhages are likely

913
 Table 2. Complications of Traumatic Hyphema when the intraocular pressure stays above
25 - 30 mm Hg for more than six days in an eye
Early glaucoma with grade III hyphema. 23 ,24,30 Blood staining
Trauma to meshwork
Obstruction of meshwork by blood or inflammatory clears, first peripherally (Fig 7), but may require
debris several months to two or three years to do
Erythrocytes SO.9,23
Normal: free or clotted
Sickled
Leukocytes and fibrin MANAGEMENT
Hemolytic glaucoma 26 (lysed and degenerated red
blood cells, hemoglobin, bilirubin, iron,
macrophages) The management of hyphema begins with
Ghost-cell glaucoma 27 (rigid, degenerated red blood examination of the patient. Examination of the
cells from vitreous hemorrhage of 7 -30 days) traumatized eye in general, and of the eye with
Phacolytic glaucoma hyphema in particular, has been detailed
Q) Pupillary block elsewhere,35.36 but a few points are Worthy of
a: "Collar-button" clot 42
w emphasis.
III
::?:
Swelling or rupture of lens Diseases or drugs that might contribute to
~ Late glaucoma abnormal bleeding or clotting, such as aspirin or
z
Traumatic fibrosis and atrophy of meshwork (with or
•
r- without postcontusion angle deformity) anticoagulants, should be asked about when
eo Hemosiderotic glaucoma 28 (fibrosis from iron in taking the patient's history. If the patient is
w black, a screening test for sickle hemoglobin or
::?: meshwork)
~
...J Ghost-cell glaucoma 27 a hemoglobin electrophoresis should be per-
o
> Peripheral anterior synechiae formed as soon as possible. 29
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Pupillary block
Posterior synechiae
A site of bleeding should be looked for, espe-
cially in the presence of persistent or black-ball
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Swelling or rupture of lens hyphema; an area of red blood in the periphery
a: Obstruction of angle by proliferation of corneal of an anterior chamber that is otherwise filled
w
III endothelium and Descemet's membrane with dark blood sometimes indicates a site of
::?: Corticosteroid-induced glaucoma
w active or continual bleeding.
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0... Blood stai ni ng of cornea
W
(f) Prolonged hypotony Gonioscopy should be avoided until the
danger of rebleeding has passed. It can be too
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>- traumatic for an eye with hyphema, and its
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o...J findings would have no bearing on initial
o to be larger than primary ones ;2,24,32 about therapy.
::?: In most _cases I prefer to avoid dilating the
...J one-third of rebleeds are of grade III severity.30
« pupil for the purpose of examining the fundus
I
l-
The visual prognosis for a hyphema of a given
I grade of severity is unchanged whether the because it is possible, although uncertain, that
0...
o hemorrhage is primary or secondary. The inci- the use of cycloplegic agents delays the absorp-
dence of glaucoma with rebleeds is at least tion of blood15 or increases the incidence of
50%.32-34 secondary hemorrhage. 33 .37 As is true of the
There is danger of damage to the optic nerve findings of gonioscopy, it is unlikely that the
if the intraocular pressure remains above 50 mm discovery of abnormalities of the posterior
Hg for more than five days;30,35 above 45 mm segment would influence early treatment. Even
Hg for more than one week,4 or above 35 mm with pupillary dilation, it is often impossible in
Hg for more than two weeks. 30 ,35 These the presence of hyphema to perform more than
guidelines apply only to relatively young and a cursory examination of the posterior segment;
healthy optic nerves. The risks are greater for as much information might be obtained by mea-
patients who are of advanced age or who have surement of visual acuity, biomicroscopic
vascular disease. The patient with a sickling examination of the media, plotting of visual
hemoglobinopathy is predisposed to develop fields, ultrasonography, or radiography to de-
stagnation of blood flow to the optic nerve and tect foreign bodies. Admittedly, there is some
so may be unable to tolerate pressures above 25 evidence that cycloplegic agents are not harm-
mm Hg for more than a day or twO. 29 ful,18 and even that they may be beneficial,t9 so
About 6 to 10% of patients with traumatic pupillary dilation is justifiable in any case in
hyphema develop late glaucoma in association which early examination of the fundus is
with postcontusion deformity of the angle. 4 ,8.23 thought to be important.
The glaucoma can appear many years after the
SITUATIONAL TREATMENT
injury and is usually associated with recession
of at least half of the angle. Practitioners should no longer feel compelled
Blood staining of the cornea is apt to develop to treat hyphema patients ritualistically with

914
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Fig 5. Histopathology of blood staining of the cornea. Dots in corneal stroma consist offree hemoglobin and small amounts of
hemosiderin (hematoxylin and eosin x 2(0) . Z
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Fig 6. Mild blood staining of the cornea, seen as a r ust-brown haze in the deep stroma (arrow).

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UJ with permission from Grayson M, Wilson FM II. Traumatic hyphema. In: Freeman HM, ed. Ocular Trauma. New York:
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Appleton-Century-Crofts, 1979; 145-9.
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o strict bed rest, binocular patching, and seda- gravitation of blood and fibrin away from the
::2:
-l tion. Controlled and prospective studies indi- pupi1. 30,35 I advise against reading but allow the
<t: cate that it makes little difference whether hos- watching of television.
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f-
I pitalized patients are confined to bed or are al-
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o lowed to ambulate, and that it is unimportant
MEDICAL TREATMENT
whether they are given one, two, or no
patches. 7,18,22 Many drugs have been used in attempts to
It has been said that patients who are hospi- treat traumatic hyphemas: miotics, cyclo-
talized within 24 hours after injury have a better plegics, adrenergics, vitamins, calcium, rutin,
prognosis than do those who enter the hospital estrogens, anticoagulants, proteolytic enzymes,
later. 24 I know of no studies that have compared corticosteroids, carbonic anhydrase inhibitors,
hospitalization with home-care, but the opinion osmotic agents, and others. 15 For nearly every
has been expressed that home-care, with study that has purported to show benefits de-
avoidance of strenuous activity, is acceptable. 15 rived from any of these agents, there has been
The need to examine the patient at least daily is at least one contradictory study that showed no
probably the strongest argument in favor of effect or even a deleterious effect,18 Havener
hospitalization. 35 reviewed the subject in detail and concluded
I hospitalize nearly all patients with traumatic that: " ... the spontaneous course of hyphema
hyphema. I patch (only) the injured eye but is totally unchanged by any form of medical
consider the application of a protective metal management. "15 I agree. The outcome depends
shield to be more important. I allow free ambu- far more on the nature and severity of the injury
lation within the hospital room but instruct the than on any medical treatment that the physi-
patient to avoid bending far forward with the cian might prescribe.
head low, lying on the side of the injury, and There is no harm in using a nontoxic, topical
lying in the prone position. I elevate the head of antibiotic, eg, sulfacetamide, for prophylaxis of
the bed 30 to 45 degrees so as to lower the pres- infection of corneal abrasion or even for
sure in the ocular vasculature and to allow for placebo effect. Otherwise, I use no medications

916
in the routine treatment of hyphema itself, but I
do not hesitate to use any medications that
might be indicated for the symptoms or compli-
cations of hyphema. When necessary, I use
cycloplegic agents for ciliary pain or for pre-
vention of posterior synechiae; miotics and
other antiglaucoma drugs for increased in-
traocular pressure; and corticosteroids for se-
vere iridocyclitis, fibrin, threatened synechiae,
or inflammatory glaucoma.
There is an unconfirmed report that the use of
oral corticosteroids reduce the incidence of
secondary hemorrhage. 38 Yet the use of topical
corticosteroids, which is known to produce
higher levels of drug in the anterior chamber,
has been found not to be beneficial in a con-
trolled, prospective study.18
Aminocaproic acid20 and tranexamic acid39
are antifibrinolytic agents. Administered orally,
each has been reported to be efficacious in pre-
venting secondary hemorrhage, presumably by
inhibiting lysis of clots in damaged vessels. The
inhibition of fibrinolysis probably also delays
absorption of hyphema. 20 These studies are as
yet unconfirmed, and the dangers of these drugs
are not well understood. Antifibrinolytic
therapy must be considered still to be experi-
mental, but it could be resorted to in difficult
cases.
Sedation to prevent rebleeding has been
largely abandoned. Light sedation itself does
not bring about restriction of activity, and
heavy sedation can cause confusion, apprehen-
sion, depression, and fatigue. Barbiturates sup-
press the rapid eye movements (REMs) of
sleep,40 but there is no evidence that this effect
prevents rebleeds. Moreover, REMs can be in-
hibited for only very limited periods of time;
their suppression can interfere with the re-
cuperative powers of sleep and can produce the
same symptoms as does loss of sleep. Ben-
zodiazepines do not affect REMs, but interfere
with stages three and four of sleep.40
Aspirin and alcohol inhibit platelet aggrega-
tion and should be avoided. 15.21
SURG leAL TREATMENT
Surgery for hyphema is not innocuous41 and
should be avoided whenever possible. Risks in-
clude damage to the cornea, iris, or lens; inad-
vertent extraction of the iris; prolapse of in-
traocular contents; renewed bleeding; increased
inflammation and formation of synechiae; and
postoperative glaucoma. Some studies have
suggested that surgical intervention may actu-
ally worsen the overall prognosis.18.37.41
The indications for surgery are said to be: (1)
uncontrolled glaucoma; (2) early blood staining
of the cornea; (3) large or total hyphemas of
more than nine days' duration; and (4) detection
of a site of active bleeding.
Elevated intraocular pressures that cannot be
controlled medically and that have reached
dangerous levels are an obvious and undisputed
indication for surgery. These levels are lower
for patients who have sickling hemoglo-
binopathy, and they should be treated with
paracentesis of the anterior chamber if the pres-
sure remains above 25 mm Hg for more than
one day.29
There is no reason to operate for blood
staining unless it is mild. Evacuation of
hyphema cannot bring about restoration of vi-
sion once the cornea has become opaque. It can
be argued that even early blood staining is not
an indication for surgery ,9 and I do not consider
the risks of surgery to be justified for this gener-
ally self-limited problem. The dangers of mild
blood staining may have been overrated,23 as
not all cases progress. Even advanced blood
staining usually clears; if it does not do so
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~
within a reasonable length of time, keratoplasty UJ
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can be performed and probably poses fewer a..
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risks than does operating for hyphema. o
A large or total hyphema is not itself an indi- i=
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cation for surgery unless there is no sign of ~
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clearing after nine days-the time after which <{
a:
peripheral anterior synechiae are likely to de- f-
velop.7 •
Z
Total hyphema virtually always causes in- o
creased intraocular pressure. If the pressure is
(fJ
-1
normal or low, especially if extensive subcon- ~
junctival hemorrhage is present, surgical explo-
ration for rupture of the globe is indicated.35
Surgery for hyphema should be preceded by
the administration of intravenous mannitol if
the intraocular pressure is elevated. Ocular
compression should be avoided.
The simplest procedures are paracentesis29 or
the release of blood through a smalllimbal inc i-
sion. 25 If these approaches are not successful,
an attempt can be made to irrigate blood from
the anterior chamber; this requires enlarging the
first incision or making a second one so as to
allow for the release of fluid and blood. Aspira-
tion can be combined with irrigation by means
of a simple two-needle technique or with the aid
of an irrigation-aspiration instrument inserted
through a single limbal incision. Ultrasonic vi-
bration of the tip is unnecessary,23 and cutting
instruments should not be used unless visu-
alization is good. Fibrinolytic agents such as
fibrinolysin34 or urokinase18 can be used for irri-
gation if the blood is partially clotted.
A large limbal incision is preferable for deal-
ing with black-ball hyphema. 23 ,35 Four or five
days after hemorrhage may be the ideal time for
intervention, as that is when the clot begins to
retract from surrounding tissues but is not yet
917
 organized and attached to themY Earlier
surgery may hold more risk for renewed bleed-
ing. Upon opening the eye, the clot may pro-
lapse spontaneously; if not, it can be rolled or
scooped gently from the eye with a cotton
swab, cellulose sponge, or lens loop. Mild pres-
sure over the inferior limbus can help to express
the clot. The clot can be extracted with a cryo-
probe,42 but great care must be taken to avoid
incorporating the iris within the ice ball. Some
practitioners,23 including myself, believe that
extraction with a cryoprobe (or with forceps) is
too dangerous to be attempted unless the posi-
tion of the iris can be visualized clearly.
Occasionally, a site of active bleeding can be
a>
c: treated.23 If it is encountered after opening the
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co anterior chamber, it may be possible to
:i' cauterize it. More often, the bleeding is from
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Z the ciliary body and cannot be reached. This
•
...... kind of bleeding might be stopped by applying
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diathermy to the overlying sclera. 23 ,43 A large
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air bubble can be put into the anterior chamber
--l to tamponade the source of bleeding; but the air
o pressure must be considerable to stop bleeding,
>
• and such pressure cannot be maintained for
asa> long because the air tends to absorb quickly.
c: Techniques have been described for the sur-
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CO
gical treatment of prolonged hypotony follow-
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ing traumatic cyclodialysis. 44
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•
>- SUMMARY
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o The most common cause of bleeding in trau-
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matic hyphema is a tear in the anterior face of
I the ciliary body, with traumatic cyclodialysis
~ being next in frequency.
c...
o The prognosis depends on the size of the
hyphema and that of any secondary hemorrhage
and, ultimately, on the severity of the injury.
The major complications are glaucoma (early or
late) and blood staining of the cornea.
Binocular patching, strict bed rest, and seda-
tion are no longer advised. No medical therapy
has been shown to be reliably beneficial for
hyphema itself, although drugs may be used as
indicated for complications . Surgical interven-
tion is hazardous and should be used only when
absolutely necessary, usually for intractable
glaucoma.
REFERENCES
1. Roy FH. Ocular Differential Diagnosis. 2nd ed.
Philadelphia: Lea and Febiger, 1975; 283-5.
2. Edwards WC , Layden WE . Traumatic hyphema : a re-
port of 184 consecutive cases . Am J Ophthalmol 1973;
75:110 - 6
918
3. Lebekhov PI, landiev 1M. Statistika i klassifikat-
siiagifemy. Oftalmol Zh 1972 ; 27:327-30.
4. Hoskins HD : Secondary glaucomas. In : Heilmann K,
Richardson KT, eds. Glaucoma Conceptions of a Dis-
ease. Pathogenesis , Diagnosis, Therapy. Philadel-
phia: WB Saunders, 1978; 376 - 89.
5. Blanton FM. Anterior chamber angle recession and
secondary glaucoma: a study of the aftereffects of
traumatic hyphemas. Arch Ophthalmol 1964;
72:39-43.
6 . Howard GM , Hutchinson BT , Frederick AR Jr .
Hyphema resulting from blunt trauma: gonioscopic,
tonographic, and ophthalmoscopic observations fol-
lowing resolution of the hemorrhage. Trans Am Acad
Ophthalmol Otolaryngol 1965; 69:294-306.
7. Read J, Goldberg MF. Comparison of medical treat-
ment for traumatic hyphema. Trans Am Acad Ophthal-
mol Otolaryngol 1974; 78799-815.
8. Yanoff M, Fine BS. Ocular Pathology. A Text and Atlas.
Hagerstown : Harper & Row, 1975; 143-8.
9. Keeney AH. Trauma of the globe, adnexa, and orbital
walls: prophylaxis and immediate therapy. In: Harley
RD, ed . Pediatric Ophthalmology. Philadelphia: WB
Saunders, 1975; 413- 28.
10. Wolff SM, Zimmerman LE. Chronic secondary
glaucoma associated with retrodisplacement of iris
root and deepening of the anterior chamber angle
secondary to contusion . Am J Ophthalmol 1962;
54:547-63.
11. Sinskey RM, Krichesky A, Henrickson R. (Abstract)
Experimental hyphema in rabbits. Am J Ophthalmol
1957; 43:292.
12 Sinskey RM, Krichesky AR. Experimental hyphema in
rabbits . III. Effect of iridectomy, iridencleisis, and tem-
porary elevation in intraocular pressure on the rate of
absorption. Am J Ophthalmol 1961; 52 :58-61.
13. Cahn PH, Havener WHo Factors of importance in trau-
matic hyphema. With particular reference to and study
of routes of absorption. Am J Ophthalmol 1963 ;
55 :591-7 .
14. HqJrven I. Erythrocyte passage into Schlemm's canal.
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