By John P. Berdahl, MD, and Prithvi Mruthyunjaya, MD
Edited by Ingrid U. Scott, MD, MPH, and Sharon Fekrat, MD
This article is from March 200
By John P. Berdahl, MD, and Prithvi Mruthyunjaya, MD
Edited by Ingrid U. Scott, MD, MPH, and Sharon Fekrat, MD
This article is from March 2007 and may contain outdated material.
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.
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 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.
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