vitreous hemorrhage

Vitreous hemorrhage

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Vitreous hemorrhage

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.

Patients with vitreous hemorrhage complain of sudden visual loss, abrupt onset of floaters that may progressively increase in severity, or occasionally, “bleeding within the eye.” Visual acuity ranges from 20/20 (6/6) to light perception. The eye is not inflamed, and clues to diagnosis are inability to see fundal details or localized collection of blood in front of the retina.

Causes of vitreous hemorrhage include retinal tear (with or without detachment), diabetic or sickle cell retinopathy, retinal vein occlusion, retinal vasculitis, neovascular age-related macular degeneration, blood dyscrasia, therapeutic anticoagulation, trauma, subarachnoid hemorrhage, and severe straining.

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

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 neovascularization. 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.


The symptoms of smaller bleeds (most bleeds are smaller bleeds) are of floaters, cobwebs, haze and shadows in the eye. There may be a red tint to the vision. Symptoms most commonly affect one eye only, although both eyes can be affected.

More severe bleeds cause haziness of vision, sometimes with blind spots or dark streaks.

The most severe bleeds cause visual loss, which can be complete, leaving the vision hazily red or black. For most people this is extremely alarming, particularly as it tends to come on very quickly with no clear explanation.


You will normally be examined with a slit lamp, a device used by opticians and ophthalmologists to look in detail at the inside of the eye. The slit lamp will allow the examiner to see if there is blood in the vitreous.

Finding the source of the bleeding may be possible with the slit lamp, although if there is a lot of blood in the vitreous humour this prevents a clear view and it may therefore be difficult to know what has happened. In this case you may have an ultrasound scan of your eye. Ultrasound can detect many causes of vitreous haemorrhage, including posterior vitreous detachment, retinal tears and detachments, tumours and foreign objects.

Sometimes an angiogram is needed. This test shows up the blood vessels in the back of the eye. This can be helpful if looking for abnormal blood vessels such as in diabetes.

Computerised tomography (CT) scanning of the eyes is useful if there is a suspicion of a penetrating injury.


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.

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