AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

Background

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. 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.

Pathophysiology

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.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

History

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 10 microliters of blood can reduce vision to hand motion.
• • The patient recognizes minimal bleeding as new multiple floaters, visual haze, smoke, shadows, or cobwebs.
  • 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 visual obstruction changes with eye or head movement and the tendency to try to look around the obstruction. In the absence of trauma, no pain is experienced with vitreous hemorrhage.

Physical

• 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 dot and blot hemorrhages of diabetic retinopathy, drusen and exudate in macular degeneration, or venous dilation in hypertensive disease and vein occlusion. Some etiologies, such as SAH, may present bilaterally.
• 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:
• • Test visual acuity in both eyes.
  • Test pupil response.
  • 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 abnormalities; this permits stronger magnification, illumination, and stereopsis. Scleral depression or use of a 3-mirror lens 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.

Causes

• Vitreous hemorrhage risk factors include diabetic retinopathy, branch or central retinal vein occlusion, retinal tears with or without detachment (especially in high myopia), PVD, and retinal artery occlusion (see Frequency).
• Trauma, including shaken baby syndrome in infants, is the leading cause of vitreous hemorrhage in young individuals.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

Other Problems to be Considered

Aneurysms (choroidal, cerebral)
Aortic arch syndromes
Arteriovenous malformations
Blood disorders (anticoagulants, thrombocytopenia, ITP)
Blunt and penetrating trauma (including shaken baby syndrome, child abuse)
Carotid-cavernous fistula
Diabetic retinopathy
Dominant (familial) exudative vitreoretinopathy
Eales disease
Hypertensive retinopathy
Hyperviscosity syndromes; chronic leukemia
Incontinentia pigment
Behçet disease
Toxocara
Norrie disease
Ocular surgery complications
Malignant choroidal melanoma
Retinoblastoma
Cavernous hemangioma of the optic nerve disc
Retinal angiomatosis
Retinal emboli (eg, talc)
Retinal telangiectasia
Retinal vasculitis, including arteriolitis
Retinal vein rupture
Retinopathy of prematurity
Retinoschisis
Sarcoidosis
Terson syndrome (SAH)
Ulcerative colitis, Crohn disease
Uveitis including pars planitis

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

Lab Studies

• No specific laboratory test exists to use in diagnosing vitreous hemorrhage. Testing to determine underlying medical conditions may be necessary once etiology of the hemorrhage is determined.
• Coagulation studies may be helpful in selected patients.

Imaging Studies

• 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.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

Emergency Department Care

• 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, such as the Early Treatment Diabetic Retinopathy Study, with vitreous hemorrhage found no benefit from discontinuing aspirin therapy as far as preventing further or recurrent hemorrhage.^{4, 5}
• 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.

Consultations

• Ophthalmologic consultation is mandatory in vitreous hemorrhage.
• A retinal specialist usually is necessary for medical and surgical intervention.
• Treatment of vitreous hemorrhage depends upon the underlying cause. In retinal tears or detachment, laser cryotherapy or scleral buckle 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 pars plana vitrectomy can restore vision (if the macular 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.
• New possibilities may be on the horizon that accelerate clot liquefaction (acetic acid), hemolysis (ultrasonography or anti–Rh-immunoglobulin), and phagocytosis (intravitreal interleukin 1).

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

Prognosis

• Prognosis depends upon the underlying cause of the hemorrhage, yet most vitreous hemorrhages resolve over time.
• Patients with diabetic retinopathy and age-related macular degeneration have the most guarded prognoses.

MULTIMEDIA

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

Media file 1:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Media file 2:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Media file 3:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Media file 4:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Media file 5:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Media file 6:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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Media file 7:  Vitreous hemorrhage. Courtesy of UT Southwestern Medical School, Department of Ophthalmology.
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REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Multimedia
• References

1. Spraul CW, Grossniklaus HE. Vitreous Hemorrhage. Surv Ophthalmol. Jul-Aug 1997;42(1):3-39. [Medline].
2. Litten M. Uber cinige vom allgemein-klinischen Standpunkt aus interessante Augenveranderungen. Berl Kline Wochenscher. 1881;18:23-27.
3. McCarron MO, Alberts MJ, McCarron P. A systematic review of Terson's syndrome: frequency and prognosis after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. Mar 2004;75(3):491-3. [Medline].
4. Chew EY, Klein ML, Murphy RP, et al. Effects of aspirin on vitreous/preretinal hemorrhage in patients with diabetes mellitus. Early Treatment Diabetic Retinopathy Study report no. 20. Arch Ophthalmol. Jan 1995;113(1):52-5. [Medline].
5. Effects of aspirin treatment on diabetic retinopathy. ETDRS report number 8. Early Treatment Diabetic Retinopathy Study Research Group. Ophthalmology. May 1991;98(5 Suppl):757-65. [Medline].
6. Flynn HW, Chew EY, Simons BD, et al. Pars plana vitrectomy in the Early Treatment Diabetic Retinopathy Study. ETDRS report number 17. The Early Treatment Diabetic Retinopathy Study Research Group. Ophthalmology. Sep 1992;99(9):1351-7. [Medline].
7. Roberts JR, Hedges JR. Clinical Procedures in Emergency Medicine. 1998:1089-119.
8. Rosen P, Baker FJ, Barkin RM. Emergency Medicine: Concepts and Clinical Practice. 1988:1033-49.
9. Rosen P, Barkin RM, Sternbach GL. Essentials of Emergency Medicine. 1991:553-66.
10. Tintinalli JE, Krome RL, Ruiz E. Emergency Medicine: A Comprehensive Study Guide. 1992:833-40.

Article Last Updated: Apr 7, 2008