Vitreous Hemorrhage Clinical Presentation

  • Author: Brian A Phillpotts, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jun 8, 2011
 

History

  • Patients with vitreous hemorrhage often present with a complaint of visual haze, floaters, cloudy vision or smoke signals, photophobia, and perception of shadows and cobwebs.
  • Small vitreous hemorrhage often is perceived as new multiple floaters, moderate vitreous hemorrhage is perceived as dark streaks, and dense vitreous hemorrhage tends to significantly decrease vision even to light perception.
  • Usually, no pain is associated with vitreous hemorrhage. Exceptions may include cases of neovascular glaucoma, severe acute ocular hypertension secondary to ghost-cell glaucoma, or trauma.
  • Ophthalmoscopic examination reveals blood within the vitreous gel and/or the anterohyaloid or retrohyaloid spaces.
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Physical

  • Vitreous hemorrhage within the Berger space tends to settle and form a crescent-shaped pool overlying the hyaloideocapsular ligament.
  • In the Cloquet canal, vitreous hemorrhage tends to delineate its inferior border and that within the retrohyaloid space caused by vitreous detachment may accumulate as a meniscus at the inferior vitreoretinal boundary, boat-shaped hemorrhage.
  • Similarly, vitreous hemorrhage within the space between the internal limiting and the nerve fiber layer may resemble that within the retrohyaloid space, except that the blood does not shift with change in the head position as may be the case with subhyaloid hemorrhage.
  • Note that sub–internal limiting membrane hemorrhage usually implies an intraretinal source of bleeding, whereas subhyaloid hemorrhage usually implies a source of bleeding anterior to the retina.
  • Vitreous hemorrhage due to Terson syndrome, anemia, Valsalva retinopathy, shaken baby syndrome, and retinal macroaneurysm rarely breaks through the internal limiting membrane or into the subretinal space.
  • Vitreous hemorrhage due to diabetic retinopathy and branch retinal vein occlusion starts anterior to the internal limiting membrane and bleeds into the vitreous.
    • The hemorrhage tends to progress through a distinct change in color from red to pink to orange to yellow white. In sub–internal limiting membrane hemorrhage, especially in sickle cell retinopathy, iridescent spots may develop with resolution of these hemorrhages. Iridescent spots are refractile, copper-colored granules representing hemosiderin-laden macrophages subjacent to the internal limiting membrane. These spots are unusual in hemorrhages anterior to the internal limiting membrane as in diabetic retinopathy or branch retinal vein occlusion.
    • Because of the presence of focal attachment between the internal limiting membrane and the retina at the central fovea area and peripheral to the posterior pole, sub–internal limiting membrane hemorrhage tends to spare the central fovea. Some attachment of the vitreous at the fovea may exist, which may explain why some preretinal hemorrhages spare the fovea.
    • On the other hand, bleeding into the vitreous body shows no definite border. In massive vitreous hemorrhages, a mild afferent pupillary defect may be observed.
  • Detailed history and physical examination are very important. History of any ocular or systemic diseases (particularly those mentioned above) as being associated with vitreous hemorrhage, including trauma, should be elicited.
  • Complete eye examination should be performed, including slit lamp examination (with gonioscopy to determine angle and iris neovascularization), intraocular pressure, and dilated fundus examination of both eyes with indirect ophthalmoscopy.
  • Scleral depression may be performed in some instances of spontaneous vitreous hemorrhage if a view of the peripheral retina is possible. In general, scleral depression is not recommended until 3-4 weeks after traumatic, vitreous hemorrhage. Scleral depression may detect a flap retinal tear.
  • In the absence of a view of the retina, B-scan ultrasonography is used to ascertain the presence of retinal detachment, retinal tear, intraocular foreign body, or intraocular tumor.
  • In some cases, the cause of vitreous hemorrhage may be ascertained by a fluorescein angiogram, if the clarity of the media allows.
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Causes

See Pathophysiology.

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Contributor Information and Disclosures
Author

Brian A Phillpotts, MD  Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine

Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Norman P Blair, MD  Director, Vitreoretinal Division, Laboratory of Retinal Circulation and Metabolism, Illinois Eye and Ear Infirmary; Professor, Department of Ophthalmology, University of Illinois at Chicago

Norman P Blair, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Diabetes Association, American Ophthalmological Society, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Jon P Gieser, MD  Assistant Professor, Department of Ophthalmology, Illinois Eye and Ear Infirmary, University of Illinois at Chicago

Jon P Gieser, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

V Al Pakalnis, MD, PhD  Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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