Vitreous Hemorrhage

Brian A Phillpotts (2013)

Overview

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.
[1]
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.
[2]
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 4-
mm 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).

Epidemiology
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%)
Trauma (12-18.8%)
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, 2-7.6% 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 (Fe
3+
) 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 hemorrhage-induced
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 Presentation

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, boat-shaped 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.
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

Differential Diagnoses

Diagnostic Considerations
ARMD, Exudative
Branch Retinal Artery Occlusion
Branch Retinal Vein Occlusion
Central Retinal Vein Occlusion
Diabetic Background Retinopathy
Diabetic Proliferative Retinopathy
Diabetic Retinopathy
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
Sarcoidosis
Uveitis, Intermediate


Workup

Laboratory 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 & Management

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
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.)
[4]

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 Summary
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

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.
Inpatient & Outpatient Medications
Depends on the suspected underlying etiology and most likely differential
diagnoses. See Differentials.
Deterrence/Prevention
A study by Smith and Steel has shown a certain amount of evidence to support
that using antivascular endothelial growth factor preoperatively in diabetic
vitrectomy can lower the occurrence of early postoperative vitreous cavity
hemorrhage.
[5]

Prognosis
Depends on the suspected underlying etiology and most likely differential
diagnoses. See Differentials


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