Vitreous hemorrhage has an incidence of seven cases per 100,000, which makes it one of the most

common causes of acutely or subacutely decreased vision. Although the diagnosis of vitreous

hemorrhage is generally straightforward, management is dictated by uncovering the underlying

etiology.

Vitreous Anatomy

The vitreous humor is 99 percent water. The remaining 1 percent is made up of collagen and hyaluronic

acid, giving it a gelatinous consistency and optical clarity. The vitreous body is defined by the internal

limiting membrane of the retina posterolaterally, by the nonpigmented epithelium of the ciliary body

anterolaterally, and by the posterior lens capsule and lens zonular fibers anteriorly. This space represents

80 percent of the eye and has a volume of approximately 4 ml. The vitreous is firmly attached to the retina

in three places: the strongest attachment is anteriorly at the vitreous base, followed by the optic nerve

head and retinal vasculature.

Mechanisms of Hemorrhage

The mechanisms of vitreous hemorrhage fall into three main categories: abnormal vessels that are

prone to bleeding, normal vessels that rupture under stress, or extension of blood from an adjacent

source. (See “Mechanisms of Vitreous Hemorrhage.”)

Abnormal vessels. Abnormal retinal blood vessels are typically the result of neovascularization due

to ischemia in diseases such as diabetic retinopathy, sickle cell retinopathy, retinal vein occlusion,

retinopathy of prematurity or ocular ischemic syndrome. As the retina experiences inadequate oxygen

supply, vascular endothelial growth factor (VEGF) and other chemotactic factors induce neovascula-

rization. These newly formed vessels lack endothelial tight junctions, which predispose them to

spontaneous bleeding. They also coexist with a fibrous component that often contracts, putting

additional stress on already fragile vessels. Also, normal vitreous traction with eye movement can

lead to rupture of these vessels.

Rupture of normal vessels. Normal vessels can rupture when sufficient mechanical force overcomes

the structural integrity of the vessel. During a posterior vitreous detachment, vitreous traction on the

retinal vasculature may compromise a blood vessel, especially at the firm attachments mentioned

above. This may happen with or without a retinal tear or detachment. However, vitreous hemorrhage

in the setting of an acute symptomatic posterior vitreous detachment should alert the clinician that

the risk of a concurrent retinal break is quite high (70–95 percent).

Blunt or perforating trauma can injure intact vessels directly and is the leading cause of vitreous

hemorrhage in people younger than 40.

A rare cause of vitreous hemorrhage is Terson’s syndrome, which refers to an extravasation of

blood into the vitreous due to a subarachnoid hemorrhage. The blood is not an extension of the

subarachnoid hemorrhage. Rather the sudden increase in intracranial pressure can cause retinal

venules to rupture.

Blood from an adjacent source. Pathology adjacent to the vitreous can also cause vitreous

hemorrhage. Hemorrhage from retinal macroaneurysms, tumors and choroidal neovascularization

can all extend through the internal limiting membrane into the vitreous. 

Signs and Symptoms

The symptoms of vitreous hemorrhage are varied but usually include painless unilateral floaters

and/or  visual loss. Early or mild hemorrhage may be described as floaters, cobwebs, haze, shadows

or a red hue. More significant hemorrhage limits visual acuity and visual fields or can cause scotomas.

Patients often say vision is worse in the morning as blood has settled to the back of the eye, covering

the macula. Patients should be questioned regarding a history of trauma, ocular surgery, diabetes,

sickle cell anemia, leukemia, carotid artery disease and high myopia.

Complete examination consists of indirect ophthalmoscopy with scleral depression, gonioscopy to

evaluate neovascularization of the angle, IOP and B-scan ultrasonography if complete view of the

posterior pole is obscured by blood. Dilated examination of the contralateral eye can help provide clues

to the etiology of the vitreous hemorrhage, such as proliferative diabetic retinopathy.

The presence of vitreous hemorrhage is not hard to detect. At the slit lamp, red blood cells may be seen

just posterior to the lens with the slit beam set “off-axis” and the microscope on the highest power. In

nondispersed hemorrhage, a view to the retina may be possible and the location and source of the

vitreous hemorrhage may be determined. Vitreous hemorrhage present in the subhyaloid space is also

known as preretinal hemorrhage. Such a hemorrhage is often boat-shaped as it is trapped in the potential

space between the posterior hyaloid and the internal limiting membrane, and settles out like a hyphema.

Dispersed vitreous hemorrhage into the body of vitreous has no defined border and can range from a few

small distinct red blood cells to total obscuration of the posterior pole.

Natural History

The blood is typically cleared from within the vitreous hemorrhage at a rate of approximately 1 percent

per day. Blood outside the formed vitreous resolves more quickly. Vitreous hemorrhage is cleared more

quickly in syneretic and vitrectomized eyes, and more slowly in younger eyes with well-formed vitreous.

The natural history of vitreous hemorrhage depends on the underlying etiology with the worst

prognoses for diabetics and AMD patients.

With the exception of proliferative vitreoretinopathy, complications of vitreous hemorrhage typically

occur if blood has been present for more than one year.

Hemosiderosis bulbi is a serious complication thought to be caused by iron toxicity as hemoglobin is

broken down. Since hemolysis occurs slowly, the iron-binding capacity of proteins in the vitreous usually

outpaces the slow rate of hemolysis, thereby avoiding hemosiderosis bulbi.

Proliferative vitreoretinopathy. After vitreous hemorrhage, proliferative vitreoretinopathy can occur.

It is thought that macrophages and chemotactic factors induce fibrovascular proliferation, which can lead

to scarring and subsequent retinal detachment.

Ghost cell glaucoma. Ghost cells are spherical, rigid, khaki-colored red blood cells filled with denatured

hemoglobin present in long-standing vitreous hemorrhage. If these cells gain access to the anterior

chamber, their shape and rigidity can block the trabecular meshwork, resulting in ghost cell glaucoma.

Hemolytic glaucoma. In hemolytic glaucoma, free hemoglobin, hemoglobin-laden macrophages and

red-blood cell debris can block the trabecular meshwork.

Treatment

The presence of a retinal detachment may be determined using ultrasonography if an adequate view

of the posterior segment is not possible. Vitrectomy is performed urgently when a retinal detachment

or break is identified. Provided the retina is attached, observation is on an outpatient basis. If the view

to the posterior pole is blocked, limitation of activities and elevation of the head of the bed while sleeping

may allow the blood to settle inferiorly and permit visualization of the superior retina where retinal breaks

most commonly occur. Retinal breaks are sealed with cryotherapy or laser photocoagulation. If a retinal

detachment has been ruled out, patients may return to normal activities.

Once the retina can be visualized, treatment is aimed at the underlying etiology as soon as possible.

If neovascularization from proliferative retinopathy is the cause, laser panretinal photocoagulation is

performed, if possible through the residual hemorrhage, to cause regression of neovascularization.

A krypton laser may aid photocoagulation as it passes through hemorrhage better than argon lasers.

An indirect laser system may also allow energy delivery to the retina around a vitreous hemorrhage.

Alternatively, in the interim, intravitreal anti-VEGF agents may induce regression of the neovascularization

until laser photocoagulation is possible. Vitrectomy is also indicated for nonclearing vitreous hemorrhage,

neovascularization of the iris and/or angle, or ghost cell glaucoma. Timing of vitrectomy depends on the

underlying etiology. New therapies, such as intravitreal injection of hyaluronidase, are currently being

studied and may provide additional treatment options in the future.