Vitreous Haemorrhage

Vitreous haemorrhage has an incidence of seven cases per 100,000, which makes it one of the most common causes of acutely or sub acutely decreased vision. Although the diagnosis of vitreous haemorrhage is generally straightforward, management is dictated by uncovering the underlying aetiology.

Vitreous Anatomy

The vitreous humour 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 fibres 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 Haemorrhage

The mechanisms of vitreous haemorrhage 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 Haemorrhage.”)

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 haemorrhage 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 haemorrhage in people younger than 40.

A rare cause of vitreous haemorrhage is Terson’s syndrome, which refers to an extravasation of blood into the vitreous due to a subarachnoid haemorrhage. The blood is not an extension of the subarachnoid haemorrhage. 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 haemorrhage. Haemorrhage from retinal macroaneurysms, tumours and choroidal neovascularization can all extend through the internal limiting membrane into the vitreous. 

Signs and Symptoms

The symptoms of vitreous haemorrhage are varied but usually include painless unilateral floaters and/or visual loss. Early or mild haemorrhage may be described as floaters, cobwebs, haze, shadows or a red hue. More significant haemorrhage 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 anaemia, leukaemia, 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 aetiology of the vitreous haemorrhage, such as proliferative diabetic retinopathy.

The presence of vitreous haemorrhage 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 haemorrhage, a view to the retina may be possible and the location and source of the vitreous haemorrhage may be determined. Vitreous haemorrhage present in the sub hyaloid space is also known as preretinal haemorrhage. Such a haemorrhage 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 haemorrhage 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 haemorrhage at a rate of approximately 1 percent per day. Blood outside the formed vitreous resolves more quickly. Vitreous haemorrhage is cleared more quickly in syneretic and vitrectomized eyes, and more slowly in younger eyes with well-formed vitreous. The natural history of vitreous haemorrhage depends on the underlying aetiology with the worst prognoses for diabetics and AMD patients.

With the exception of proliferative vitreoretinopathy, complications of vitreous haemorrhage 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 haemoglobin is broken down. Since haemolysis occurs slowly, the iron-binding capacity of proteins in the vitreous usually outpaces the slow rate of haemolysis, thereby avoiding hemosiderosis bulbi.

Proliferative vitreoretinopathy. After vitreous haemorrhage, 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-coloured red blood cells filled with denatured haemoglobin present in long-standing vitreous haemorrhage. If these cells gain access to the anterior chamber, their shape and rigidity can block the trabecular meshwork, resulting in ghost cell glaucoma.

Haemolytic glaucoma. In haemolytic glaucoma, free haemoglobin, haemoglobin-laden macrophages and red-blood cell debris can block the trabecular meshwork.