Vitreous Hemorrhage in Emergency Medicine 

Since men of medicine began studying the human body, anatomists and pathologists have been intrigued by the mysterious, gelatinous substance filling the eyeball. Vitreous body comprises four fifths of the globe, averaging 4 mL in an adult. Vitreous is 99% water, with collagen and hyaluronic acid comprising the remaining 1%. These components give vitreous its specific gel-like form.

Emergency physicians are rarely called upon to diagnose and treat diseases of the vitreous, but sometimes their timely diagnosis and referral to a specialist can be vision-saving. Frequently, even the suspicion of vitreoretinal disease mandates referral to an eye surgeon with special training in problems of the eye's posterior pole.

One such ophthalmologic emergency is a vitreous hemorrhage, as shown in the images below. Vitreous hemorrhage is defined as the presence of extravasated blood within the space outlined by the zonular fibers and posterior lens capsule anteriorly, the nonpigmented epithelium of the ciliary body laterally, and the internal limiting membrane of the retina (lamina limitans interna) posteriorly and posterolaterally. Because distinguishing blood between the internal limiting membrane and the retina's nerve fiber layer (called a subinternal limiting membrane hemorrhage) from retrohyaloid (subhyaloid) hemorrhage is not always possible, theses conditions are all considered to be types of vitreous hemorrhage.

For related CME activities, see CME - Issues in Vitreoretinal Disease and CME - AAO 2007: Retinal Disease. Also see Medscape's Ophthalmology specialty page.

Vitreous is a clear, gelatinous, and avascular substance, filling the space bound by the lens, retina, and optic disc. A layer of cells, termed the internal limiting membrane, coats the inner surface of the retina, separating it from the vitreous and forming a potential space (ie, subhyaloid space).

Since healthy vitreous is relatively inelastic and impervious to cells and debris, it plays an essential role in maintaining the transparency and form of the eye. If vitreous is removed, the eye loses its mechanical and structural integrity and therefore collapses. If the vitreous is replaced with saline (as in some forms of vitreous surgery), cellular matter and debris may freely migrate into the optical pathway.

Since the vitreous is avascular a vitreous hemorrhage describes the juxtaposition of blood within a bloodless gel. Vitreous has firm attachments to 3 important areas of the inner eye.

• First, at the most anterior portion and termination of the retina (ie, ora serrata), a circular band approximately 4 mm wide forms the vitreous base. This is the strongest of all attachments and maintains its strength throughout life. Any traction of this area is transmitted to the adjacent peripheral retina.
• The second attachment is at the circular zone of the optic nerve head. This area progressively weakens with age and can separate with posterior vitreous detachment (PVD). As a result, one often can observe a feathery ring (ie, Weiss ring) following PVD.
• The third area of firm attachment occurs to the retina along the course of the major retinal vessels. Vitreous traction along the vessels may lead to partial-thickness retinal breaks (ie, retinal pits) or full-thickness breaks with a bridging vessel. Tractional forces, whether traumatic or from pathologic vascularization of the retina, result in hemorrhage into the vitreous.

Perivascular tractional forces along any of these attachments, whether traumatic or from pathologic vascularization of the retina, may result in hemorrhage into or behind the vitreous. If bleeding has occurred in the subhyaloid space, it appears boat shaped on the surface of the retina, forming a superior meniscus in an upright patient but changes with position. Blood within the space between the internal limiting membrane and the nerve fiber layer is under tension and does not shift with position of the patient's head. In contrast, blood in the vitreous body shows no characteristic borders, clots rapidly, and clears slowly, about 1% per day. The slow clearing leading to the persistent presence of blood may lead to either hemosiderosis bulbi or glaucoma.^[1]

One of the earliest clinical descriptions of vitreous hemorrhage was found by Litten in 1881 in persons suffering subarachnoid hemorrhage.^[2] This uncommon but interesting mechanism of vitreous hemorrhage is called Terson syndrome, whereby vitreous hemorrhage occurs as a result of abrupt intracranial (ie, subarachnoid) bleeding. Between 10 and 40% of all patients with subarachnoid hemorrhage (SAH) have an associated vitreous hemorrhage or Terson syndrome. Frequently bilateral, SAH often occurs in younger individuals and is a poor prognostic indicator. Some studies have suggested that compared with patients with SAH alone, patients with both subarachnoid and vitreous bleeding are 4.8 times more likely to die.^[3]

The exact mechanism for Terson vitreous hemorrhage is unknown, although the sudden increased pressure associated with an intracranial hemorrhage is believed to be transmitted via the optic nerve to retinal venules and capillaries, rupturing them.

Frequency

United States

The prevalence of vitreous hemorrhage corresponds to the frequency of the underlying disease processes with which it is associated. In the United States, the population-based incidence of spontaneous vitreous hemorrhage is approximately 7 cases per 100,000.

The 3 most common causes of vitreous hemorrhage are proliferative diabetic retinopathy, posterior vitreous detachment (PVD) with or without retinal tears, and ocular trauma (eg, shaken baby syndrome); together these account for 60-89% of all cases. Less common causes include branch or central retinal vein occlusion, proliferative sickle cell retinopathy, retinal microaneurysm, age-related macular degeneration, and subarachnoid hemorrhage (Terson syndrome).

Rare causes of vitreous detachment include Valsalva-maneuver–induced retinopathy, complications of eye surgery, orbital malignancies, inborn or acquired blood dyscrasias, vasculitides, and hypertensive retinopathy. Any cause of peripheral neovascularization may result in vitreous hemorrhage (see Differentials), but trauma is the leading cause of vitreous hemorrhage in young people.

Race

Race, sex, and age of the patient presenting with vitreous hemorrhage correspond to the incidence of the underlying disease. Examples include aneurysmal SAH among women, diabetes and sickle cell disease among black individuals; macular degeneration among elderly white individuals (which can lead to subretinal neovascularization and breakthrough bleeding into the vitreous); and individuals with high myopia, who have an increased risk of retinal tears, detachment, and associated vitreous hemorrhage.