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Symptoms ⬇

Sudden, painless loss of vision or sudden appearance of black spots, cobwebs, or haze in the vision.

Signs ⬆ ⬇

(See Figure 11.13.1.)

Critical

In severe VH, the red fundus reflex may be absent, and there may be limited or no view to the fundus. Red blood cells may be seen in the anterior vitreous (or anterior chamber). In mild VH, there may be a partially obscured view to the fundus. Chronic VH has a yellow ocher appearance from hemoglobin breakdown.

Other

A mild RAPD is possible in the setting of dense hemorrhage. Depending on the etiology, there may be other fundus abnormalities.

11-13.1 Vitreous and preretinal hemorrhage due to proliferative diabetic retinopathy.

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Differential Diagnosis ⬆ ⬇

  • Vitritis (white blood cells in the vitreous): Usually not sudden onset; anterior or posterior uveitis may also be present. No red blood cells are seen in the vitreous. See 12.3, POSTERIOR UVEITIS.
  • RD: May occur without a VH, but the symptoms may be similar. In VH due to RD, the peripheral retina may be obscured on indirect ophthalmoscopy requiring B-scan US to detect the detachment. See 11.3, RETINAL DETACHMENT.

Etiology ⬆ ⬇

  • Diabetic retinopathy: Usually history of diabetes with diabetic retinopathy. Diabetic retinopathy is usually evident in the contralateral eye. In VH due to PDR, the peripheral retina is often visible on indirect ophthalmoscopy. See 11.12, DIABETIC RETINOPATHY.
  • PVD: Common in middle-aged or elderly patients. Usually patients note floaters and flashing lights. See 11.1, POSTERIOR VITREOUS DETACHMENT.
  • Retinal break: Commonly superior in cases of dense VH. This may be demonstrated by scleral depression and, if poor view, B-scan US. See 11.2, RETINAL BREAK.
  • RD: May be diagnosed by B-scan US if the retina cannot be viewed on clinical examination. See 11.3, RETINAL DETACHMENT.
  • Retinal vein occlusion (usually a BRVO): Commonly occurs in older patients with a history of high blood pressure. See 11.9, BRANCH RETINAL VEIN OCCLUSION.
  • Exudative age-related macular degeneration (AMD): Usually with advanced CNV. Poor vision before the VH as a result of the underlying macular disease. Macular drusen and/or other findings of AMD are found in the contralateral eye. B-scan US may aid in the diagnosis. See 11.17, NEOVASCULAR OR EXUDATIVE (WET) AGE-RELATED MACULAR DEGENERATION.
  • Sickle cell disease: May have peripheral retinal neovascularization in the contralateral eye, typically in a “sea fan” configuration and salmon color. See 11.20, SICKLE CELL RETINOPATHY (INCLUDING SICKLE CELL DISEASE, ANEMIA, AND TRAIT).
  • Trauma: By history.
  • Valsalva: By history.
  • Intraocular tumor: May be visible on ophthalmoscopy or B-scan US. See 5.13, MALIGNANT MELANOMA OF THE IRIS and 11.36, CHOROIDAL NEVUS AND MALIGNANT MELANOMA OF THE CHOROID.
  • Subarachnoid or subdural hemorrhage (Terson syndrome): Frequently bilateral preretinal or VHs may occur. A severe headache usually precedes the fundus findings. Coma may occur.
  • Others: Ruptured arterial macroaneurysm, Eales Disease, Coats disease, retinopathy of prematurity, retinal capillary angiomas of von Hippel–Lindau syndrome, congenital prepapillary vascular loop, retinal cavernous hemangioma, HTN, radiation retinopathy, anterior segment hemorrhage because of an intraocular lens, bleeding diathesis, hematologic malignancy, etc. See specific sections.
NOTE:

In infancy and childhood, consider birth trauma, child abuse (e.g., shaken baby syndrome), congenital X-linked retinoschisis, pars planitis, bleeding dyscrasias, and hematologic malignancies.

Work Up ⬆ ⬇

Workup
  1. History: Any ocular or systemic diseases? Trauma?
  2. Complete ocular examination, including slit lamp examination with undilated pupils to check for iris neovascularization, IOP measurement, and dilated fundus examination of both eyes by using indirect ophthalmoscopy. In cases of spontaneous VH, scleral depression is performed if a retinal view can be obtained.
  3. When no retinal view can be obtained, B-scan US is performed to detect an associated RD or intraocular tumor. Flap RTs may be detected with scleral depression and may be seen on B-scan US (elevated flap).
  4. IVFA may aid in defining the etiology, although the quality of the angiogram depends on the density of the hemorrhage. Additionally, it may be useful to highlight abnormalities in the contralateral eye.

Treatment ⬆ ⬇

  1. If the etiology of VH is not known and a retinal break or an RD or both cannot be ruled out (i.e., there is no known history of one of the diseases mentioned previously, there are no changes in the contralateral eye, and the fundus is obscured by a total VH), close observation versus vitrectomy are options.
  2. Observation:
    • No heavy lifting, no straining, no bending. Keep head of bed elevated. This reduces the chance of recurrent bleeding and allows blood to settle inferiorly, permitting a view of the superior peripheral fundus, a common site for possible retinal breaks.
    • Eliminate aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and other anticlotting agents unless medically necessary.
    • The underlying etiology is treated as soon as possible (e.g., retinal breaks are sealed with cryotherapy or laser photocoagulation, detached retinas are repaired, and proliferative retinal vascular diseases are treated with anti-VEGF therapy or laser photocoagulation).
  3. Vitrectomy:
    • VH accompanied by RD or RT on B-scan US.
    • Nonclearing VH. Because two-thirds of patients with an idiopathic, fundus-obscuring hemorrhage will have RTs or an RD, early vitrectomy should be considered.
    • VH with neovascularization of the iris.
    • Hemolytic or ghost cell glaucoma.

Follow Up ⬆

If observation is elected, the patient is evaluated daily for the first 2 to 3 days. If a total, dense VH persists, and the etiology remains unknown, vitrectomy should be considered.