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You are in: eMedicine Specialties > Ophthalmology > VITREOUS

Hemorrhage, Vitreous
Article Last Updated: Feb 13, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous

References

Author: Brian A Phillpotts, MD, Former Vitreo-Retinal Service Director, Former

Program Director, Clinical Assistant Professor, Department of Ophthalmology,
Howard University College of Medicine
Brian A Phillpotts is a member of the following medical societies: American
Academy of Ophthalmology, American Diabetes Association, American Medical
Association, and National Medical Association
Coauthor(s): Norman P Blair, MD, Director, Vitreoretinal Division, Laboratory of
Retinal Circulation and Metabolism, Illinois Eye and Ear Infirmary; Professor,
Department of Ophthalmology, University of Illinois at Chicago; Jon P Gieser, MD,
Assistant Professor, Department of Ophthalmology, Illinois Eye and Ear Infirmary,
University of Illinois at Chicago
Editors: Vytautas A Pakainis, MD, Chief of Ophthalmology, Dorn Veterans
Administration Medical Center, Professor of Ophthalmology, Ophthalmology,
University of South Carolina School of Medicine; Simon K Law, MD, PharmD,
Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of
Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare
Center, West Los Angeles; Steve Charles, MD, Director of Charles Retina Institute;
Clinical Professor, Department of Ophthalmology, University of Tennessee College
of Medicine; Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman
Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri; Hampton
Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University
of Arkansas for Medical Sciences
Author and Editor Disclosure
Synonyms and related keywords: vitreous hemorrhage, retinal vascular tears,
neovascularization of the retina, retinal neovascularization, retinal detachment,
proliferative diabetic retinopathy, posterior vitreous detachment

INTRODUCTION
Section 2 of 10
Authors and Editors
Introduction

Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

Background
Vitreous hemorrhage is the extravasation of blood into one of the several potential
spaces formed within and around the vitreous body. This condition may result
directly from retinal tears or neovascularization of the retina, or it may be related to
bleeding from preexisting blood vessels in these structures.
The vitreous body is bounded posterolaterally by the internal limiting membrane of
the retina, anterolaterally by the nonpigmented epithelium of the ciliary body, and
anteriorly by the lens zonular fibers and posterior lens capsule. The retrolental
space of Erggelet and the canal of Petit are potential spaces. These 2 spaces are
located between the anterior hyaloid membrane, the posterior lens capsule, and the
orbiculoposterocapsular portion of the zonular fibers. The hyaloideocapsular
ligament separates them from each other.
The Cloquet canal and the bursa premacularis are fluid-filled spaces within the
formed vitreous into which blood can enter during vitreous hemorrhage. The
aqueous-filled space anterior to the formed vitreous is called the canal of Hannover.
This space is located between the orbiculoanterocapsular and posterocapsular
portions of the zonular fibers.
Historically, anatomists do not consider it a part of vitreous humor; however,
hemorrhage into this space is considered functionally as vitreous hemorrhage. The
same is true for bleeding into the retrohyaloid or subhyaloid spaces and for sub
internal limiting membrane hemorrhage.
On April 20, 1970, the first pars plana vitrectomy for the treatment of nonclearing
vitreous hemorrhage was performed by Machemer. Prior to pars plana vitrectomy,
the removal of nonclearing vitreous hemorrhage was attempted by excising
vitreous gel through the pupillary aperture using cellulose sponges and scissors via
a corneoscleral incision, which was coined "open-sky" vitrectomy by Kasner. The
procedure was frequently unsuccessful, and patients often had a permanent
reduction in vision.

Pathophysiology
The vitreous has 3 strong attachment areas with the retina. The strongest
attachment straddles the most anterior area of the retina (ora serrata) where a 4mm circular band forms the vitreous base. Traction at the vitreous base usually is
transmitted to the adjacent peripheral retina. The next strong attachment of the
vitreous is at the circular zone around the optic nerve head. This zone becomes
progressively weakened with increasing age, and it becomes easily separated with
posterior vitreous detachment.
In the adult, the vitreous body volume is approximately 4 mL, which is 80% of the
globe. The content of the vitreous is 99% water, and the remaining 1% mostly is
composed of collagen and hyaluronic acid. Additionally, there are a few other
soluble components such as ions, proteins, and trace cells. These components
account for the gelatinous but clear nature of the vitreous.
The vitreous is avascular and inelastic. Pathological mechanisms of vitreous
hemorrhage can include hemorrhage from diseased retina, traumatic insult, and/or
spread of hemorrhage into the retina and vitreous from any other intraocular
sources.
Given the history and physical findings, it also may be reasonable to consider
extraocular etiologies such as leukemia. Usually, coagulation disorders or
anticoagulant therapy does not cause vitreous hemorrhage; however, bleeding from
abnormal new vessels or rupture of normal retinal vessels from direct or indirect
trauma frequently is associated with vitreous hemorrhage. Bleeding from
neovascular and fragile vessels in proliferative diabetic retinopathy, proliferative
sickle cell retinopathy, ischemic retinopathy secondary to retinal vein occlusion, and
retinopathy of prematurity are among the most common pathological causes of
vitreous hemorrhage.
The most common pathogenesis of bleeding in this group of disorders is believed
to be retinal ischemia causing the release of angiogenic vasoactive factors, most
notably vascular endothelial growth factor (VEGF), basic fibroblast growth factors
(bFGF), and insulin-like growth factor (IGF). The second most frequent pathological
mechanism for vitreous hemorrhage is tearing of the retinal vessels caused by
either a break in the retina or detachment of the posterior vitreous, while the cortical
vitreous is adherent to the retinal vessels. In addition, patients with sickle cell
retinopathy may show a salmon-patch hemorrhage caused by blowout in the vessel
wall following abrupt occlusion in the arterioles by aggregated sickled red blood
cells.
Other less common pathological mechanisms of vitreous hemorrhage include
subretinal bleeding with secondary extension into the vitreous cavity.

Age-related macular degeneration and choroidal melanoma are the two leading
causes of vitreous hemorrhage secondary to breakthrough bleeding. Terson
syndrome is subarachnoid hemorrhage associated with vitreous bleeding caused
by rupture of retinal venules and/or capillaries as a result of a sudden increase in
intracranial pressure (which is transmitted to the retinal vasculature via the optic
nerve).
Reports have shown that about 33% of patients with subarachnoid hemorrhage
may have associated intraocular hemorrhage, and approximately 6% of patients
have vitreous hemorrhage. In Terson syndrome, branches of the central retinal vein
or the central retinal vein itself is the most common source of intraocular bleeding.
Terson syndrome occurs mostly in younger individuals (age 30-50 y).

Frequency
United States
The prevalence of vitreous hemorrhage tends to parallel the frequency of the
causative disease. In general, the cause-prevalence of vitreous hemorrhage
depends on the study population, mean age of the patients, and geographical
region where the study is conducted. In adults, proliferative diabetic retinopathy is
the most frequent cause of vitreous hemorrhage, 31.5-54% in the United States,
6% in London, and 19.1% in Sweden.
The other causes of vitreous hemorrhage include the following:

Retinal tear (11.4-44%)

Posterior vitreous detachment with retinal vascular tear (3.7-11.7%)
Rhegmatogenous retinal detachment (7-10%)
Proliferative sickle cell retinopathy (0.2-5.9%)
Macroaneurysm (0.6-7.4%)
Age-related macular degeneration (0.6-4.3%)
Terson syndrome (0.5-1.0%)
Trauma (12.0-18.8%)
Retinal neovascularization as a result of branch or central retinal vein
occlusion (3.5-16%)

Rare causes of vitreous hemorrhage account for about 6.4-18% of vitreous

hemorrhage. In several studies, 2.0-7.6% of the hemorrhage could not be attributed
to a specific cause.
The leading cause of vitreous hemorrhage in young people is trauma.
Congenital retinoschisis and pars planitis also may cause vitreous hemorrhage in

both children and adults.

Mortality/Morbidity
The complications of vitreous hemorrhage include hemosiderosis bulbi with
photoreceptor toxicity, glaucoma, severe floaters, and myopic shift in infants.

In hemosiderosis bulbi, iron (Fe3+) is released during hemoglobin

breakdown. This occurs intracellularly in macrophages with subsequent
storage as ferritin or hemosiderin. Alternatively, the catabolism of
hemoglobin can take place extracellularly and the released iron binds to
vitreous proteins with iron-binding capacity, such as lactoferrin and
transferrin. The vitreous contains 13 times more iron-binding proteins
relative to the serum, with a physiological saturation of the total iron-binding
capacity of about 35%. Given the slow clearance of blood in the vitreous, the
persistence of intact red blood cells and the slow hemolysis in the vitreous,
the amount of iron released from hemoglobin is a relatively small fraction of
that available at any given time.
The exact mechanism of postvitreous hemorrhage retinal damage has not
been completely elucidated. It currently is believed that this damage may be
caused by direct or indirect toxicity of iron. For example, iron enters cell wall
membranes via secondary lysosomes with the liberation of contained
enzymes causing indirect damage. Iron also has been implicated in the
release of mitogenic growth factor from macrophages following phagocytosis
of blood from vitreous hemorrhage.
Overall, patients with long-standing vitreous hemorrhage and relatively
normal retina tend to have good visual acuity. The vitreous hemorrhageinduced glaucoma is secondary to the blockade of the trabecular meshwork
by formed ghost cells due to long-standing blood cells in the vitreous. Ghost
cells are small, khaki-colored, spherical, more rigid cells, which develop from
long-standing red blood cells in the vitreous where there is a relatively low
oxygen tension. In hemolytic glaucoma, the trabecular meshwork is blocked
by red blood cell debris, free hemoglobin, and hemoglobin-laden
macrophages. In hemosiderotic glaucoma, the iron derived from vitreous
hemorrhage binds to the trabecular meshwork mucopolysaccharide causing
endothelial cell damage with possible complications of sclerosis and
obliteration of the intertrabecular spaces. This form of glaucoma often
presents after years of recurrent vitreous hemorrhage.
Myopic shift and amblyopia have been reported to follow long-standing
vitreous hemorrhage in infants, especially in those younger than 2 years.
In high myopic persons, the risk of retinal tears, detachment, and associated
vitreous hemorrhage is increased.
In general, iron-related toxicity may become clinically apparent in instances
of significant long-standing vitreous hemorrhage, often with histopathologic

signs of hemosiderosis.

Race
The demographics of vitreous hemorrhage correspond to the incidence of the
underlying disease with which it is associated.

In blacks, diabetes and sickle cell disease tend to be the most common.
In elderly whites with vitreous hemorrhage, retinal vascular tears and
neovascularization caused by proliferative diabetic retinopathy and branch
retinal vein occlusion are more common. In the same population, macular
degeneration and breakthrough bleeding into the vitreous are not infrequent.

Sex
Corresponds to the incidence of the underlying disease with which it is associated

Age
Corresponds to the incidence of the underlying disease with which it is associated

CLINICAL
Section 3 of 10
Authors and Editors
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Clinical
Differentials
Workup
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Medication
Follow-up
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References

History

Patients with vitreous hemorrhage often present with a complaint of visual

haze, floaters, cloudy vision or smoke signals, photophobia, and perception
of shadows and cobwebs.

Small vitreous hemorrhage often is perceived as new multiple floaters,

moderate vitreous hemorrhage is perceived as dark streaks, and dense
vitreous hemorrhage tends to significantly decrease vision even to light
perception.
Usually, no pain is associated with vitreous hemorrhage. Exceptions may
include cases of neovascular glaucoma, severe acute ocular hypertension
secondary to ghost-cell glaucoma, or trauma.
Ophthalmoscopic examination reveals blood within the vitreous gel and/or
the anterohyaloid or retrohyaloid spaces.

Physical

Vitreous hemorrhage within the Berger space tends to settle and form a
crescent-shaped pool overlying the hyaloideocapsular ligament.
In the Cloquet canal, vitreous hemorrhage tends to delineate its inferior
border and that within the retrohyaloid space caused by vitreous detachment
may accumulate as a meniscus at the inferior vitreoretinal boundary, boatshaped hemorrhage.
Similarly, vitreous hemorrhage within the space between the internal limiting
and the nerve fiber layer may resemble that within the retrohyaloid space,
except that the blood does not shift with change in the head position as may
be the case with subhyaloid hemorrhage.
Note that subinternal limiting membrane hemorrhage usually implies an
intraretinal source of bleeding, whereas subhyaloid hemorrhage usually
implies a source of bleeding anterior to the retina.
Vitreous hemorrhage due to Terson syndrome, anemia, Valsalva retinopathy,
shaken baby syndrome, and retinal macroaneurysm rarely breaks through
the internal limiting membrane or into the subretinal space.
Vitreous hemorrhage due to diabetic retinopathy and branch retinal vein
occlusion starts anterior to the internal limiting membrane and bleeds into
the vitreous.

The hemorrhage tends to progress through a distinct change in color

from red to pink to orange to yellow white. In subinternal limiting
membrane hemorrhage, especially in sickle cell retinopathy,
iridescent spots may develop with resolution of these hemorrhages.
Iridescent spots are refractile, copper-colored granules representing
hemosiderin-laden macrophages subjacent to the internal limiting
membrane. These spots are unusual in hemorrhages anterior to the
internal limiting membrane as in diabetic retinopathy or branch retinal
vein occlusion.
Because of the presence of focal attachment between the internal
limiting membrane and the retina at the central fovea area and
peripheral to the posterior pole, subinternal limiting membrane
hemorrhage tends to spare the central fovea. Some attachment of the
vitreous at the fovea may exist, which may explain why some

preretinal hemorrhages spare the fovea.

o On the other hand, bleeding into the vitreous body shows no definite
border. In massive vitreous hemorrhages, a mild afferent pupillary
defect may be observed.
Detailed history and physical examination are very important. History of any
ocular or systemic diseases (particularly those mentioned above) as being
associated with vitreous hemorrhage, including trauma, should be elicited.
Complete eye examination should be performed, including slit lamp
examination (with gonioscopy to determine angle and iris
neovascularization), intraocular pressure, and dilated fundus examination of
both eyes with indirect ophthalmoscopy.
Scleral depression may be performed in some instances of spontaneous
vitreous hemorrhage if a view of the peripheral retina is possible. In general,
scleral depression is not recommended until 3-4 weeks after traumatic,
vitreous hemorrhage. Scleral depression may detect a flap retinal tear.
In the absence of a view of the retina, B-scan ultrasonography is used to
ascertain the presence of retinal detachment, retinal tear, intraocular foreign
body, or intraocular tumor.
In some cases, the cause of vitreous hemorrhage may be ascertained by a
fluorescein angiogram, if the clarity of the media allows.

Causes
See Pathophysiology.

DIFFERENTIALS
Section 4 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

ARMD, Exudative
Branch Retinal Artery Occlusion
Branch Retinal Vein Occlusion
Central Retinal Vein Occlusion
Eales Disease

Leukemias
Macroaneurysm
Melanoma, Choroidal
Melanoma, Ciliary Body
Melanoma, Iris
Neovascular Membranes, Subretinal
Neovascularization, Choroidal
Ocular Ischemic Syndrome
Ocular Manifestations of Syphilis
Presumed Ocular Histoplasmosis Syndrome
Retinitis Pigmentosa
Retinoblastoma
Retinopathy of Prematurity
Retinopathy, Diabetic, Background
Retinopathy, Diabetic, Proliferative
Retinopathy, Hemoglobinopathies
Sarcoidosis
Uveitis, Intermediate

Other Problems to be Considered

Most commonly encountered differential diagnoses in decreasing order of
frequency include the following:
Proliferative diabetic retinopathy
Posterior vitreous detachment
Trauma (blunt or penetrating, including shaken baby syndrome/child abuse)
Retinal tear
Retinal vein occlusion
Hypertensive retinopathy
Subarachnoid hemorrhage (Terson syndrome)
Avulsed retinal vessels
Age-related macular degeneration
Radiation retinopathy
Macroaneurysms
Others rare causes of vitreous hemorrhage include the following:
Complications of surgical procedures
Retinal laser photocoagulation
Intruding (scleral erosion) scleral buckle
Trabeculectomy
Globe perforation during retrobulbar or peribulbar surgery/anesthesia
Intraocular lens implantation or removal

Neovascularization from cataract wound

Tumors
Malignant choroidal melanoma
Melanocytoma of optic nerve disc
Astrocytic hamartoma of the retina
Retinoblastoma
Cavernous hemangioma of optic nerve disc
Vascular/neovascular
Coats disease/retinal telangiectasia
Retinopathy of prematurity (ROP)
Ocular ischemic syndrome
Branch retinal artery occlusion
Central retinal artery occlusion
Retinal angiomatosis
Retinal vasculitis
Hyperviscosity syndrome
Sarcoid posterior uveitis
Persistent hyaloid artery
Congenital prepapillary
Vascular loop venous stasis retinopathy
Dominant (familial) exudative vitreoretinopathy
Incontinentia pigmenti
Norrie disease
Inflammation
Behet disease
Presumed ocular histoplasmosis syndrome
Eales disease
Uveitis (including pars planitis)
Syphilitic retinitis
Dermatomyositis
Systemic lupus erythematosus (SLE)
Toxocara
Hematologic disorders
Thrombocytopenia
Idiopathic thrombocytopenia purpura
Thrombotic thrombocytopenic purpura
Leukemia

Hemophilia
Disseminated intravascular coagulation
Protein C deficiency
Antiphospholipid antibodies
Von Willebrand syndrome
Miscellaneous causes
Talc retinopathy
Retinitis
Pigmentosa Valsalva retinopathy

WORKUP
Section 5 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

Lab Studies

Consider ordering laboratory studies as per the suspected underlying

etiology and its corresponding differential diagnosis. See Differentials.

Imaging Studies

Consider ordering imaging studies as per the suspected underlying etiology

and its corresponding differential diagnosis.

With CT scan and/or MRI, exclude globe perforation, intraocular

foreign body, avulsed optic nerve, intraocular tumor, displaced scleral
buckle, and intraocular lens materials. See Differentials.
Ocular B-scan ultrasonography is used when the media is opacified
enough to preclude a complete and clear (including view of the ora

serrata) funduscopic examination.

TREATMENT
Section 6 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

Medical Care

Treatment is directed at the underlying cause, if known.

On rare occasions, such as unreliable/noncompliant patients with

vitreous hemorrhage complicated with severe hyphema, patients may
be admitted to the hospital for close observation. Otherwise, most
patients are monitored closely on an outpatient basis with emphasis
on cooperation with treatment instructions.
Bed rest with the head of the bed elevated 30-45 with occasional
bilateral patching to allow the blood to settle inferiorly, allowing a view
of the superior peripheral fundus
Avoid drugs such as aspirin and other anticlotting agents when
necessary.

Surgical Care

The goal is to treat the underlying cause as quickly as possible. For

example, retinal breaks are closed by laser photocoagulation or cryotherapy
(unlike cryotherapy, laser photocoagulation can close the compromised
vessel in addition to the retinal tear); detached retinas are reattached with
surgery; and proliferative retinal vascular diseases are treated with laser
photocoagulation or cryotherapy (when there is no view of the retina).
Indications for surgical removal of the vitreous blood include the following:

Vitreous hemorrhage associated with detached retina

o
o

Long-standing vitreous hemorrhage with duration greater than 2-3

months (Vitrectomy for isolated vitreous hemorrhage (eg, without
retinal detachment) may be performed before 2-3 months in patients
with juvenile-onset diabetes, patients with bilateral vitreous
hemorrhage, children in the amblyogenic age range, and/or when
retinal traction is suspected.)
Vitreous hemorrhage associated with rubeosis
Vitreous hemorrhage associated with hemolytic or ghost-cell
glaucoma

Consultations

Depends on the suspected underlying etiology and most likely differential

diagnoses. See Differentials.
Retinal specialist

MEDICATION
Section 7 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication

Follow-up
Miscellaneous
References

Medical therapy depends on the suspected underlying etiology and the most likely
differential diagnosis. See Differentials. Avoid drugs such as aspirin and other
anticlotting agents when necessary.

FOLLOW-UP
Section 8 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

Further Outpatient Care

Initially, patients with vitreous hemorrhage are monitored daily for 2-5 days
to rule out retinal tear or detachment, then every 1-2 weeks for spontaneous
clearing. However, in the event that the dense vitreous hemorrhage persists
without known underlying cause, a B-scan ultrasonography should be
serially performed.

In/Out Patient Meds

Depends on the suspected underlying etiology and most likely differential

diagnoses. See Differentials.

Prognosis

Depends on the suspected underlying etiology and most likely differential

diagnoses. See Differentials.

MISCELLANEOUS
Section 9 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

Medical/Legal Pitfalls

Patients should be examined carefully to rule out the possibility that a retinal
detachment is involved.

REFERENCES
Section 10 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References

Abok K, Blomquist E, Ericsson J, Brunk U. Macrophage radiosensitivity in

culture as a function of exposure to ionic iron. Virchows Arch B Cell Pathol
Incl Mol Pathol. 1983;42(2):119-29. [Medline].
Ackerman J, Goldstein M, Kanarek I. Spontaneous massive vitreous

hemorrhage secondary to thrombocytopenia. Ophthalmic

Surg. Sep 1980;11(9):636-7. [Medline].
Benson WE, Wirostko E, Spalter HF. The effects of inflammation on
experimentally induced vitreous hemorrhage. Arch
Ophthalmol. Dec 1969;82(6):822-6. [Medline].
Burke JM. Vitreal superoxide and superoxide dismutase after hemorrhagic
injury: the role of invasive cells. Invest Ophthalmol Vis
Sci. Apr 1981;20(4):435-41. [Medline].
Butner RW, McPherson AR. Spontaneous vitreous hemorrhage. Ann
Ophthalmol. Mar 1982;14(3):268-70. [Medline].
Campbell DG. Ghost cell glaucoma following
trauma. Ophthalmology. Nov 1981;88(11):1151-8. [Medline].
Campbell DG, Essigmann EM. Hemolytic ghost cell glaucoma. Further
studies. Arch Ophthalmol. Nov 1979;97(11):2141-6. [Medline].
Clarkson JG. The ocular manifestations of sickle-cell disease: a prevalence
and natural history study. Trans Am Ophthalmol Soc. 1992;90:481504. [Medline].
Dana MR, Werner MS, Viana MA, Shapiro MJ. Spontaneous and traumatic
vitreous hemorrhage. Ophthalmology. Sep 1993;100(9):1377-83. [Medline].
Ernest JT, Stern WH. Internal limiting membrane detachment in branch
retinal vein obstruction. Am J Ophthalmol. Aug 1974;78(2):324-6. [Medline].
Fenton RH, Hunter WS. Hemolytic glaucoma. Surv
Ophthalmol. Aug 1965;10(4):355-60. [Medline].
Ferrone PJ, de Juan E Jr. Vitreous hemorrhage in infants. Arch
Ophthalmol. Sep 1994;112(9):1185-9. [Medline].
Foos RY. Vitreoretinal juncture; topographical variations. Invest
Ophthalmol. Oct 1972;11(10):801-8. [Medline].
Forrester JV, Lee WR, Williamson J. The pathology of vitreous hemorrhage.
I. Gross and histological appearances. Arch
Ophthalmol. Apr 1978;96(4):703-10. [Medline].
Frankel CA, Pastore DJ. Idiopathic thrombocytopenic purpura with
intracranial hemorrhage and vitreous hemorrhage. Clin Pediatr
(Phila). Dec 1990;29(12):725-8. [Medline].
Gagliano DA, Goldberg MF. The evolution of salmon-patch hemorrhages in
sickle cell retinopathy. Arch Ophthalmol. Dec 1989;107(12):18145. [Medline].
Goff MJ, McDonald HR, Johnson RN, et al. Causes and treatment of
vitreous hemorrhage. Compr Ophthalmol Update. May-Jun 2006;7(3):97111. [Medline].
Greenwald MJ, Weiss A, Oesterle CS, Friendly DS. Traumatic retinoschisis
in battered babies. Ophthalmology. May 1986;93(5):618-25. [Medline].
Gutierrez Diaz A, Jimenez Carmena J, Ruano Martin F, et al. Intraocular
hemorrhage in sudden increased intracranial pressure (Terson
syndrome). Ophthalmologica. 1979;179(3):173-6. [Medline].
Hayreh SS, Rojas P, Podhajsky P, et al. Ocular neovascularization with
retinal vascular occlusion-III. Incidence of ocular neovascularization with

retinal vein occlusion. Ophthalmology. May 1983;90(5):488-506. [Medline].

Hayreh SS, Edwards J. Ophthalmic arterial and venous pressures. Effects of
acute intracranial hypertension. Br J Ophthalmol. Oct 1971;55(10):64963. [Medline].
Hiscott P, Waller HA, Grierson I, et al. The extracellular matrix of reparative
tissue in the vitreous: fibronectin production in proliferative diabetic
retinopathy membranes. Eye. 1993;7 (Pt 2):288-92. [Medline].
Jampol LM, Ebroon DA, Goldbaum MH. Peripheral proliferative
retinopathies: an update on angiogenesis, etiologies and management. Surv
Ophthalmol. May-Jun 1994;38(6):519-40. [Medline].
Kadrmas EF, Pach JM. Vitreous hemorrhage and retinal vein rupture. Am J
Ophthalmol. Jul 1995;120(1):114-5. [Medline].
Kasner D. Past and present indications for "open sky" vitrectomy. Advances
in Vitreous Surgery. 1976;Jun 2:127-9.
Kono T, Higashi M. The pathogenesis of long-standing preretinal membrane
induced by vitreous hemorrhage. Nippon Ganka Gakkai
Zasshi. May 1988;92(5):857-63. [Medline].
Kono T. Reaction of retinal glial cells to form preretinal membrane induced
by vitreous hemorrhage. Nippon Ganka Gakkai
Zasshi. Oct 1987;91(10):911-22. [Medline].
Lincoff H, Kreissig I, Wolkstein M. Acute vitreous haemorrhage: a clinical
report. Br J Ophthalmol. Jun 1976;60(6):454-8. [Medline].
Lindgren G, Sjodell L, Lindblom B. A prospective study of dense
spontaneous vitreous hemorrhage. Am J Ophthalmol. Apr 1995;119(4):45865. [Medline].
Machemer R, Buettner H, Norton EW, Parel JM. Vitrectomy: a pars plana
approach. Trans Am Acad Ophthalmol Otolaryngol. Jul-Aug 1971;75(4):81320. [Medline].
McGahan MC, Fleisher LN. Inflammation-induced changes in the iron
concentration and total iron- binding capacity of the intraocular fluids of
rabbits. Graefes Arch Clin Exp Ophthalmol. 1988;226(1):27-30. [Medline].
Miller-Meeks MJ, Bennett SR, Keech RV, Blodi CF. Myopia induced by
vitreous hemorrhage. Am J Ophthalmol. Feb 15 1990;109(2):199203. [Medline].
Morris DA, Henkind P. Relationship of intracranial, optic-nerve sheath and
retinal hemorrhage. Am J Ophthalmol. Nov 1967;64(5):853-9. [Medline].
Morse PH, Aminlari A, Scheie HG. Spontaneous vitreous hemorrhage. Arch
Ophthalmol. Oct 1974;92(4):297-8. [Medline].
Muller PJ, Deck JH. Intraocular and optic nerve sheath hemorrhage in cases
of sudden intracranial hypertension. J Neurosurg. Aug 1974;41(2):1606. [Medline].
Rabb MF, Gagliano DA, Teske MP. Retinal arterial macroaneurysms. Surv
Ophthalmol. Sep-Oct 1988;33(2):73-96. [Medline].
Russell SR, Hageman GS. Hemorrhagic detachment of the internal limiting
membrane after penetrating ocular injury. Retina. 1992;12(4):34650. [Medline].

Sebag J. Age-related changes in human vitreous structure. Graefes Arch

Clin Exp Ophthalmol. 1987;225(2):89-93. [Medline].
Tawara A. Transformation and cytotoxicity of iron in siderosis bulbi. Invest
Ophthalmol Vis Sci. Feb 1986;27(2):226-36. [Medline].
Van Bockxmeer FM, Martin CE, Constable IJ. Iron-binding proteins in
vitreous humour. Biochim Biophys Acta. Jul 5 1983;758(1):17-23. [Medline].
Williams TD. Preretinal/intraretinal hemorrhages: a photographic essay. J
Am Optom Assoc. May 1988;59(5):397-400. [Medline].
Winslow RL, Taylor BC. Spontaneous vitreous hemorrhage: etiology and
management. South Med J. Nov 1980;73(11):1450-2. [Medline].

Hemorrhage, Vitreous excerpt

Article Last Updated: Feb 13, 2007