Since the earliest days of the study of medicine and the human body, anatomists and pathologists have been intrigued by the mysterious, gelatinous substance filling a majority of the volume of the eye. The 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 abnormalities within the vitreous mandates referral to an eye surgeon with special training in the diagnosis and treatment of vitreoretinal disease of the eye.
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 actually within the vitreous from bleeding between the internal limiting membrane and the retina's nerve fiber layer (called a subinternal limiting membrane hemorrhage) and from preretinal hemorrhages (those between the internal limiting membrane and the vitreous) is not always possible by the ED physician, these conditions are all considered types of vitreous hemorrhage.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
The 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, lines the inner surface of the retina, separating it from the vitreous and forming one side of a potential space between it and the vitreous (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 the vitreous is removed surgically and replaced with saline (as in some forms of vitreous surgery), cellular matter and debris may more freely migrate into the optical pathway than if there is natural vitreous.
Since the vitreous is avascular, a vitreous hemorrhage describes the invasion of blood into a bloodless gel. Vitreous has firm attachments to 2 important areas of the inner eye.
First, at the anterior most portion and termination of the retina (ie, ora serrata), a circular band posterior to the retinal termination, approximately 4 mm wide, forms the vitreous base. This is the strongest of all attachments of the vitreous to its surrounding structures and maintains its strength throughout life. Any pulling forces (traction) on the vitreous are transmitted to the adjacent peripheral retina at the vitreous base.
The second attachment is posteriorly at the margin of the optic nerve, where the vitreous is attached in a circle of approximately 2 mm in diameter. During the aging process, the vitreous normally liquefies and shrinks. This shrinkage may reach a certain stage at which this attachment of the vitreous gives way and the vitreous detaches from its posterior attachment at the margin of the optic nerve. This is called a posterior vitreous detachment (PVD) or posterior vitreous separation. The prior attachment of the vitreous to the optic nerve head can often be seen as a feathery ring (ie, Weiss ring) following PVD. A PVD is present in approximately 50% of people at age 60 years.
Tractional forces at either of these attachments may result in hemorrhage within or underneath the vitreous. If bleeding has occurred in the subhyaloid space, it appears boat shaped on the surface of the retina, forming a superior straight line in an upright patient but changing with the position of the patient. Blood within the space between the internal limiting membrane and the nerve fiber layer is under tension and does not shift with the position of the patient's head. In contrast, blood in the vitreous body shows no characteristic borders, may clot in parts, and clears slowly, at about 1% per day.
One of the earliest clinical descriptions of vitreous hemorrhage was authored by the German ophthalmologist Litten in 1881 in persons with subarachnoid hemorrhage (SAH).[1] This uncommon but interesting mechanism of vitreous hemorrhage is called Terson syndrome, named after the French ophthalmologist who described it 19 years later; vitreous hemorrhage occurs as a result of abrupt intracranial (ie, subarachnoid) bleeding with anterior dissection of blood under the arachnoid coat of the optic nerve into the eye.
Between 10 and 40% of all patients with SAH have an associated vitreous hemorrhage, which is termed Terson syndrome. If Terson syndrome is bilateral, its presence represents a poor prognostic indicator of SAH. 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.[2]
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 persons per year.
The most common causes of vitreous hemorrhage are proliferative diabetic retinopathy, vitreoretinal traction with retinal tears, PVD with or without retinal tears, severe choroidal neovascularization with breakthrough bleeding into the vitreous, and ocular trauma (eg, shaken baby syndrome, postsurgical eyes, automobile injuries, direct trauma to the eye). Together, these account for the majority of all cases. Less common causes include branch or central retinal vein occlusion, sickle cell retinopathy, age-related macular degeneration, intraocular tumors, retinopathy of prematurity, the leukemias, acute retinal necrosis, HIV-related retinopathy, and some types of uveitis. Retinal neovascularization of any cause can result in vitreous hemorrhage.
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/choroidal 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.
Patient history, both medical and ocular, is essential in the emergency department evaluation of vitreous hemorrhage. Assessing and documenting the patient's vision prior to symptoms of hemorrhage is crucial. Underlying eye disease often provides clues to the cause of hemorrhage.
Patients with acute vitreous hemorrhage frequently seek emergency care because the loss of vision is dramatic. Visual acuity varies with the degree of hemorrhage, but even a small amount of blood can reduce vision to hand motion.
The patient recognizes minimal bleeding as new multiple floaters, visual haze, smoke, shadows, cobwebs, or visual blurring. Moderate hemorrhage may be described graphically as 1 or more dark streaks that subsequently break up into numerous, minute black spots. Dense hemorrhage can reduce vision to the light perception level.
Patients may report that the visual obstruction changes with eye or head movement and that they may tend to attempt to look around the obstruction. In the absence of trauma, no pain is experienced with vitreous hemorrhage unless it is accompanied by acute angle closure glaucoma from the blood-filled vitreous pushing the iris-lens diaphragm forward.
A complete eye examination is indicated for both eyes. Examining the uninvolved eye may provide clues to the underlying cause of hemorrhage in the involved eye, such as the dot and blot hemorrhages seen with diabetic retinopathy, drusen and exudate in macular degeneration, or venous dilation in hypertensive disease and vein occlusion. Some etiologies, such as SAH, may manifest as bilateral vitreous hemorrhage.
Once diagnosis of vitreous hemorrhage is confirmed, ophthalmologic consultation is indicated to determine the causes and appropriate intervention.
A complete eye examination includes the following:
Visual acuity testing of each eye individually
Pupillary response testing
Slit-lamp examination: Fresh blood is identified readily by adjusting the slit beam to a tangential position and viewing the anterior vitreous directly behind the lens. Retrolenticular hemorrhage may be easily visualized.
Direct ophthalmoscopy: With direct ophthalmoscopy, a variable loss of fundus detail is present with floating debris, which often is recognized as red debris. Old hemorrhage undergoes syneresis (ie, degenerates), loses color (turns orange or whitish yellow), and settles inferiorly. Resolving hemorrhage may leave an iridescent spot or refractile hemosiderin copper-colored granules.
Indirect ophthalmoscopy: Use of this technique usually requires expert training and is best left to the trained ophthalmologist. Indirect ophthalmoscopy is the only way to evaluate the eye for peripheral retinal abnormalities. Scleral depression is required to exclude retinal tears of the periphery.
Preretinal (ie, subhyaloid) hemorrhage commonly is observed on the fundus upon examination of shaken infants and has a characteristic meniscus that changes direction with head position.
Vitreous hemorrhage risk factors include diabetic retinopathy, branch or central retinal vein occlusion, retinal tears with or without detachment (especially in high myopia), posterior vitreous detachment, and retinal artery occlusion.
Trauma, including shaken baby syndrome in infants, is the leading cause of vitreous hemorrhage in young individuals.
No specific laboratory test is used in diagnosing vitreous hemorrhage. Testing to determine underlying medical conditions may be necessary once the etiology of the hemorrhage is determined. Coagulation studies may be helpful in selected patients.
Ultrasonography is the mandatory imaging technique when the view of the fundus is obstructed by hemorrhage, corneal opacification, or cataract. Experienced ultrasonographers can confirm if the retina is attached, if an intraocular foreign body is present, and if a PVD exists.
In an observational study, ED physicians have been shown to be able to reliably evaluate for retinal detachments using bedside ultrasonography.[3] However, in this study, vitreous hemorrhages were sometimes misidentified as retinal detachments. Although acute vitreous hemorrhages appear as minimal echogenic structures, over time they can become more organized and appear as a linear structure.
Distinguishing between retinal detachments and vitreous hemorrhages with ophthalmic ultrasonography is based on 3 distinct findings, as follows:
Retinal detachments can be followed posteriorly to the optic disc.
Unlike retinal detachments, vitreous hemorrhages remain horizontal when the patient moves their eye side to side.
Vitreous hemorrhages are often seen in the middle section of the posterior eye.
ED treatment of vitreous hemorrhage involves documentation with history and physical examination. Ophthalmologic consultation then is required.
Emergent consultation is required if hemorrhage has resulted from trauma or abuse or if retinal tear or detachment is suspected.
In medical conditions such as diabetes, peripheral neovascularization, or sickle cell disease, obtain a consultation within 48 hours and treat the patient as an outpatient.
Discharge instructions must include limiting physical activity and sleeping in an upright position.
Anticoagulants and other antiplatelet agents may need to be stopped immediately, but this must be considered on an individual patient basis weighing the risks and benefits of such cessation carefully with patients and their physicians. Studies in diabetic retinopathy with vitreous hemorrhage, such as the Early Treatment Diabetic Retinopathy Study, found no benefit from discontinuing aspirin therapy as far as preventing further or recurrent hemorrhage.[4, 5, 6]
Do not discharge patients from the ED until a time and date for the consultation is available.
Follow-up care should confirm that the patient saw a consultant.
Ophthalmologic consultation is mandatory in vitreous hemorrhage.
A retinal specialist usually is necessary for surgical intervention.
Treatment of vitreous hemorrhage depends on the underlying cause. In symptomatic retinal tears with vitreous hemorrhage, laser or cryotherapy is generally indicated. In retinal detachment, pars plana vitrectomy or scleral buckling surgery is indicated. With underlying medical diseases, treat the patient conservatively with upright positioning for sleep to enhance settling of the hemorrhage.
With the exception of trauma and retinal detachment, close observation for 1-2 weeks allows time for spontaneous clearing of some hemorrhage, but it may take several months for vision to return, depending on the specific case and the underlying disease process. Surgical intervention with hemorrhage removal by pars plana vitrectomy can restore vision (if the macula is healthy) when spontaneous clearing does not occur over a period of months.
Bilateral patching to limit eye movements and placing the patient in an upright position may accelerate the layering out of the blood and speed resolution.
Andrew A Dahl, MD, FACS, Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Disclosure: Nothing to disclose.
Additional Contributors
Richard S Krause, MD, Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences
Disclosure: Nothing to disclose.
Acknowledgements
Gregory L Larkin, MD, MS, MSPH, FACEP Professor, Department of Emergency Medicine, Yale University School of Medicine
Gregory L Larkin MD, MD, MS, MSPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Society for Bioethics and Humanities, Association for the Advancement of Automotive Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Douglas Lavenburg, MD Clinical Professor, Department of Emergency Medicine, Christiana Care Health Systems
Douglas Lavenburg, MD is a member of the following medical societies: American Society of Cataract and Refractive Surgery
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